Targeting the Origins of Inflammation in Post-Traumatic Osteoarthritis

创伤后骨关节炎（PTOA）的特征是由各种关节损伤引起的进行性关节软骨侵蚀，其严重程度从非接触性前交叉韧带撕裂（ACLT）到关节内骨折（IAF）不等。即使在IAF的情况下，软骨和软骨细胞的直接损伤通常只占关节表面的百分之几。然而，这种局部病变可能随着时间的推移而扩大；一种与受伤软骨释放介质有关的现象。然而，软骨侵蚀也发生在原来受损的软骨之外，这表明滑膜液中携带的分解代谢因子引发了未受损软骨的退变。因此，以预防创伤性炎症为中心的干预对于减少创伤性软骨损失具有很大的潜力。关节软骨的机械损伤导致损伤部位的软骨细胞死亡和基质变性，随着时间的推移，相邻软骨也会发生这种情况。传递组织损伤信号的基质碎片和细胞碎片(统称为

Post-traumatic osteoarthritis (PTOA) is characterized by progressive articular cartilage erosion initiated by a variety of joint injuries ranging in severity from non-contact anterior cruciate ligament tears (ACLT) to intra-articular fracture (IAF). Even in the case of IAF, the immediate damage to cartilage and chondrocytes typically amounts to only a few percent of the joint surface. Yet, such localized lesions can expand over time; a phenomenon associated with release of mediators from injured cartilage. However, cartilage erosion also occurs away from originally damaged cartilage, indicating that catabolic factors carried in synovial fluid initiate degeneration in undamaged cartilage. Thus, an intervention centered on preventing trauma-induced inflammation holds great potential for reducing trauma-induced cartilage loss. Mechanical injuries to articular cartilage cause the death of chondrocytes and matrix degeneration in injury sites and, over time, in adjacent cartilage. Matrix fragments and cell debris signaling tissue damage (known collectively as